The effect of calcium and prostaglandin inhibitors on the intestinal fluid response to heat-stable enterotoxin of escherichia coli

D. Denee Thomas, Floyd C. Knoop

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27 Citations (Scopus)

Abstract

The role of calcium and prostaglandins in the intestinal fluid response to Escherichia coli heat-stable enterotoxin (ST) was investigated in infant mice. Drugs that inhibit calcium uptake-cromolyn sodium, diltiazem, and nifedipine-caused a significant (P < 0.02, P <0.02, and P <0.01, respectively) decrease in the fluid response when administered with ST. The effect of cromolyn sodium and nifedipine was dose-dependent; both agents were effective when administered 30 min before toxin challenge. Inhibitors of prostaglandin synthesis -quinacrine hydrochloride and zomepirac sodium -caused a significant (P< 0.05 and P< 0.02, respectively) reduction in the fluid response when administered with or 30 min before ST. The fluid response to cyclic 8-bromoguanosine 3',5'-monophosphate or to nitroprusside, which directly activates guanylate cyclase, was not altered by inhibitors of calcium uptake or prostaglandin synthesis. These observations indicate that calcium and prostaglandins are involved in the initial events that result in an intestinal fluid response to E. coli ST.

Original languageEnglish (US)
Pages (from-to)141-147
Number of pages7
JournalJournal of Infectious Diseases
Volume145
Issue number2
DOIs
StatePublished - Jan 1 1982

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Prostaglandin Antagonists
Enterotoxins
Hot Temperature
Escherichia coli
Prostaglandins
Calcium
Cromolyn Sodium
Nifedipine
Quinacrine
Diltiazem
Guanylate Cyclase
Nitroprusside
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Infectious Diseases

Cite this

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abstract = "The role of calcium and prostaglandins in the intestinal fluid response to Escherichia coli heat-stable enterotoxin (ST) was investigated in infant mice. Drugs that inhibit calcium uptake-cromolyn sodium, diltiazem, and nifedipine-caused a significant (P < 0.02, P <0.02, and P <0.01, respectively) decrease in the fluid response when administered with ST. The effect of cromolyn sodium and nifedipine was dose-dependent; both agents were effective when administered 30 min before toxin challenge. Inhibitors of prostaglandin synthesis -quinacrine hydrochloride and zomepirac sodium -caused a significant (P< 0.05 and P< 0.02, respectively) reduction in the fluid response when administered with or 30 min before ST. The fluid response to cyclic 8-bromoguanosine 3',5'-monophosphate or to nitroprusside, which directly activates guanylate cyclase, was not altered by inhibitors of calcium uptake or prostaglandin synthesis. These observations indicate that calcium and prostaglandins are involved in the initial events that result in an intestinal fluid response to E. coli ST.",
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N2 - The role of calcium and prostaglandins in the intestinal fluid response to Escherichia coli heat-stable enterotoxin (ST) was investigated in infant mice. Drugs that inhibit calcium uptake-cromolyn sodium, diltiazem, and nifedipine-caused a significant (P < 0.02, P <0.02, and P <0.01, respectively) decrease in the fluid response when administered with ST. The effect of cromolyn sodium and nifedipine was dose-dependent; both agents were effective when administered 30 min before toxin challenge. Inhibitors of prostaglandin synthesis -quinacrine hydrochloride and zomepirac sodium -caused a significant (P< 0.05 and P< 0.02, respectively) reduction in the fluid response when administered with or 30 min before ST. The fluid response to cyclic 8-bromoguanosine 3',5'-monophosphate or to nitroprusside, which directly activates guanylate cyclase, was not altered by inhibitors of calcium uptake or prostaglandin synthesis. These observations indicate that calcium and prostaglandins are involved in the initial events that result in an intestinal fluid response to E. coli ST.

AB - The role of calcium and prostaglandins in the intestinal fluid response to Escherichia coli heat-stable enterotoxin (ST) was investigated in infant mice. Drugs that inhibit calcium uptake-cromolyn sodium, diltiazem, and nifedipine-caused a significant (P < 0.02, P <0.02, and P <0.01, respectively) decrease in the fluid response when administered with ST. The effect of cromolyn sodium and nifedipine was dose-dependent; both agents were effective when administered 30 min before toxin challenge. Inhibitors of prostaglandin synthesis -quinacrine hydrochloride and zomepirac sodium -caused a significant (P< 0.05 and P< 0.02, respectively) reduction in the fluid response when administered with or 30 min before ST. The fluid response to cyclic 8-bromoguanosine 3',5'-monophosphate or to nitroprusside, which directly activates guanylate cyclase, was not altered by inhibitors of calcium uptake or prostaglandin synthesis. These observations indicate that calcium and prostaglandins are involved in the initial events that result in an intestinal fluid response to E. coli ST.

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